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Year : 2021  |  Volume : 69  |  Issue : 4  |  Page : 1114--1115

Long Vertebral Arteritis and Cerebellar Infarction caused by Suspected Giant Cell Arteritis

Yuya Kobayashi, Shunichi Sato, Ryota Takamatsu, Wataru Ishii 
 Department of Neurology, Nagano Red Cross Hospital, Wakasato, Nagano, Japan

Correspondence Address:
Yuya Kobayashi
Department of Neurology, Nagano Red Cross Hospital, 5-22-1, Wakasato, Nagano, 380-8582
Japan




How to cite this article:
Kobayashi Y, Sato S, Takamatsu R, Ishii W. Long Vertebral Arteritis and Cerebellar Infarction caused by Suspected Giant Cell Arteritis.Neurol India 2021;69:1114-1115


How to cite this URL:
Kobayashi Y, Sato S, Takamatsu R, Ishii W. Long Vertebral Arteritis and Cerebellar Infarction caused by Suspected Giant Cell Arteritis. Neurol India [serial online] 2021 [cited 2022 May 25 ];69:1114-1115
Available from: https://www.neurologyindia.com/text.asp?2021/69/4/1114/325359


Full Text



A 79-year-old Japanese man was admitted with pulsatile headache and ataxia. He had polymyalgia rheumatica and had been taking prednisolone (12 mg/day). Magnetic resonance imaging (MRI) revealed cerebellar infarction and right vertebral artery stenosis [Figure 1]a and [Figure 1]b. Aspirin and argatroban were started. MRI on day 7 revealed new cerebellar infarction. His erythrocyte sedimentation rate was 26 mm/h, and he had pulsatile headache, suggesting giant cell arteritis (GCA) related to polymyalgia rheumatica. The right vertebral artery was enhanced on MRI, proving arteritis [Figure 1]c. Arterial dissection was suspected, but it was ruled out because of circumferential wall thickening and absence of false lumen formation. All collagen-related markers including ANCA-related disease were negative. Biopsy of the temporal artery revealed no histological finding. This case did not meet GCA criteria[1] because it was based on temporal arteritis; however, GCA was strongly suspected. We increased the amount of prednisolone to 30 mg/day recommended dose.[2] He had no recurrence; however, the finding on MRI persisted. No further immunosuppressive therapy was administered because the patient was elderly and had experienced bleeding due to intestinal candidiasis.{Figure 1}

In this case, a long stenotic lesion developed only in the vertebral artery, and it was resistant to steroid therapy. GCA occurs in only 0.15% cerebral infarction cases.[3] Postcirculatory cerebral infarction with headache suggests arterial dissection. In patients with GCA, vertebrobasilar infarction is the most common type.[4] GCA should be suspected, and contrast MRI is recommended. The main strategy is to use corticosteroids. However, steroid treatment is ineffective or causes a new infarction in some cases.[4] Other immunosuppressive therapies, such as cyclophosphamide, tocilizumab, and methotrexate, have also been reported.[4]

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Hunder G, Bloch D, Michel B, Stevens MB, Arend WP, Calabrese LH, et al. The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum 1990;33:1122-8.
2Watelet B, Samson M, de Boysson H, Bienvenu B. Treatment of giant-cell arteritis, a literature review. Mod Rheumatol 2017;27:747-54.
3Thielen KR, Wijdicks EF, Nichols DA. Giant cell (temporal) arteritis: Involvement of the vertebral and internal carotid arteries. Mayo Clinic Proc 1998;73:444-6.
4Haisa T, Tsuda T, Hagiwara K, Kikuchi T, Seki K. Vertebrobasilar infarction related to giant cell (temporal) arteritis: Case report. Neurol Med Chir (Tokyo) 2015;55:95-100.